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ABSTRACT: LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function

PROVIDER: PRJNA149931 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR387732.fastq.gz	Fastqsanger.gz
	SRR387733.fastq.gz	Fastqsanger.gz
	SRR387734.fastq.gz	Fastqsanger.gz
	SRR387735.fastq.gz	Fastqsanger.gz
	SRR389293.fastq.gz	Fastqsanger.gz

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LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function

Project description:This SuperSeries is composed of the following subset Series: GSE34030: LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [RNA-Seq] GSE34295: LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq] Refer to individual Series

2011-12-09 | E-GEOD-34296 | biostudies-arrayexpress

LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq]

Project description:We have determined the cistrome and transcriptome for the nuclear receptor liver receptor homolog-1 (LRH-1) in the exocrine pancreas. Chromatin immunoprecipitation (ChIP)-seq and RNA-seq analyses reveal that LRH-1 directly induces expression of genes encoding digestive enzymes and secretory and mitochrondrial proteins. LRH-1 cooperates with the pancreas transcription factor 1-L complex (PTF1-L) in regulationg exocrine pancreas-specific gene expression. Elimination of LRH-1 in adult mice reduced the concentration of several lipases and proteases in pancreatic fluid and impaired pancreatic fluid secretion in response to cholecystokinin. Thus, LRH-1 is a key regulator of the exocrine pancreas-specific transcriptional network required for the production and secretion of pancreatic fluid. input and Lrh1 ChIP

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LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq]

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Project description:Early postnatal overnutrition causes persistent dysregulation of endocrine pancreas function. We used genome-scale DNA methylation profiling in the suckling-period small litter (SL) mouse model to test whether this occurs via persistent epigenetic changes in pancreatic islets. Although SL islets showed DNA methylation changes directly after weaning and in adulthood, few of these were present at both ages, contrary to our hypothesis. Most interestingly, we discovered that genomic regions that are hypermethylated in exocrine relative to endocrine pancreas tend to gain methylation in islets during aging. Focusing on a subset of genes relevant to β cell function, we showed that these methylation differences are strongly correlated with expression. Together, our results provide the novel insight that DNA methylation changes that occur as islets age indicate an overall epigenetic drift toward the exocrine pancreas epigenome. These concerted shifts in the islet methylome could contribute to the age-associated decline in endocrine pancreas function. Pancreatic islets were isolated from P21/P180 SL or C mice. To ensure purity of islets, 3 rounds of manual picking were performed in each samples. Whole pancreas samples, ~98% of which is exocrine pancreas, were used as exocrine pancreas. There are 5 mice per group.

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